Norharman
Norharman is a good inhibitor on MAO A and MAO B isozymes.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to
24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com
The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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Related and Featured Products
Cancer Letters, 1999,143(2):139-143.
Quantification of the co-mutagenic β-carbolines, norharman and harman, in cigarette smoke condensates and cooked foods.[Reference:
WebLink]
METHODS AND RESULTS:
Co-mutagenic β-carbolines, such as Norharman and harman, were quantified in mainstream and sidestream smoke condensates of six Japanese brands of cigarettes, and also in 13 kinds of cooked foods, using a combination of blue cotton treatment and HPLC. Norharman and harman were detected in all the cigarette smoke condensate samples. Their levels in the mainstream smoke case were 900–4240 ng per cigarette for Norharman, and 360–2240 ng for harman, and in sidestream smoke, 4130–8990 ng for Norharman and 2100–3000 ng for harman. These β-carbolines were also found to be present in all the cooked food samples, at levels of 2.39–795 ng for Norharman and 0.62–377 ng for harman per gram of cooked food.
CONCLUSIONS:
The observed concentrations are much higher than those found for mutagenic and carcinogenic heterocyclic amines (HCAs), suggesting that humans are exposed to Norharman and harman in daily life to a larger extent than to HCAs.
Life Sciences, 2006, 78(8):0-802.
Human monoamine oxidase enzyme inhibition by coffee and β-carbolines norharman and harman isolated from coffee.[Reference:
WebLink]
Monoamine oxidase (MAO) is a mitochondrial outer-membrane flavoenzyme involved in brain and peripheral oxidative catabolism of neurotransmitters and xenobiotic amines, including neurotoxic amines, and a well-known target for antidepressant and neuroprotective drugs. Recent epidemiological studies have consistently shown that coffee drinkers have an apparently lower incidence of Parkinson's disease (PD), suggesting that coffee might somehow act as a purported neuroprotectant.
METHODS AND RESULTS:
In this paper, “ready to drink” coffee brews exhibited inhibitory properties on recombinant human MAO A and B isozymes catalyzing the oxidative deamination of kynuramine, suggesting that coffee contains compounds acting as MAO inhibitors. MAO inhibition was reversible and competitive for MAO A and MAO B. Subsequently, the pyrido-indole (β-carboline) alkaloids, Norharman and harman, were identified and isolated from MAO-inhibiting coffee, and were good inhibitors on MAO A (harman and Norharman) and MAO B (Norharman) isozymes.
CONCLUSIONS:
β-carbolines isolated from ready-to-drink coffee were competitive and reversible inhibitors and appeared up to 210 μg/L, confirming that coffee is the most important exogenous source of these alkaloids in addition to cigarette smoking. Inhibition of MAO enzymes by coffee and the presence of MAO inhibitors that are also neuroactive, such as β-carbolines and eventually others, might play a role in the neuroactive actions including a purported neuroprotection associated with coffee consumption.
European Journal of Pharmacology, 2002, 441(1-2):115-125.
The levels of norharman are high enough after smoking to affect monoamineoxidase B in platelets.[Reference:
WebLink]
Epidemiological studies suggest that smoking reduces the risk for Parkinson's disease. It has been hypothesized that inhibition of monoamineoxidase contributes to this action.
METHODS AND RESULTS:
The present study examined the contribution of the beta-carbolines Norharman, an inhibitor of monoamineoxidase B, and harman, an inhibitor of monoamineoxidase A, which are present in high concentrations in tobacco smoke to the protective action. Nineteen active smokers and five nonsmokers smoked one and two cigarettes. The levels of Norharman and harman increased in plasma from smokers and nonsmokers. Ex vivo saturation kinetic experiments revealed that the baseline affinity constant of monoamineoxidase in platelets from smokers was higher than that of nonsmokers in contrast to the maximum turnover rate, which did not differ. Acute smoking affected the monoamineoxidase in nonsmokers only.
CONCLUSIONS:
It is discussed that inhibition of both isoforms of monoamineoxidase is necessary for the neuroprotection and that both Norharman and harman play an important role.
